Endocarditis

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Introduction

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Endocarditis is defined as an inflammation of the cardiac endocardium. The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis). It is usually a result of a bacteraemia or pyaemia, spread from adjaent myocardium is rare. It occurs in all species and is more common in cattle, pigs and sheep than dogs and cats.

Bacterial endocarditis. Courtesy of A. Jefferies

Organisms commonly isolated include:

Pathophysiology

Vegetative Endocarditis

Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Bacteremia is essential for the development of endocarditis. Once bacteria colonize the valvular endocardium, vegetative lesions composed of platelets and fibrin are formed on the valves. Progression to rupture of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetant or both. Death usually results from either embolisation of the vegetative material or congestive heart failure due to significant valvular damage.

Vegetative endocarditis (dog). Courtesy of T. Scase

UlcerativeEndocarditis

Commonly seen along with renal failure in dogs.Uraemia irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the subendocardial tissue with deposition of glycosaminoglycans. This may progress to a necrotising endocarditis and, in extreme cases, left atrial rupture. If renal sufficieny is re-established then healing of the endocardial lesion is possible.

Species differences

  • Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. COmmon underlying causes include Liver abcesses, traumatic reticulitis, metritis, mastitis, navel ancesses and 'joint ill'. Congestive right sided failure is manifested as ascites (including bottle jaw) and embolisation to the lungs. Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
  • Horse: Lesions occur mainly on the mitral valve. The site of sepsis is often not identified but may be a sequale to septic jugular thrombophlembitis.
  • Pig and dog: Lesions occur particularly on the mitral valve (71% of cases in dogs), perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.

Signalment

Clinical Signs

Diagnosis

Laboratory findings

Echocardiography

Radiography

Electrogcardiogram (ECG)

Treatment

Prognosis

References

from clinical

Infective Endocarditis

Bacterial endocarditis. Courtesy of A. Jefferies

Signalment

Present in small animals:

Dogs: (uncommon); Males & Large Breeds (e.g. German Shepherd) most affected

Cats: (rare)


Present in large animals:

Cattle: (common); Adult cattle

Swine: (very common); Young pigs

Horse: (uncommon); Males more affected


Diagnosis

History & Clinical Signs

-Sings of Embolization:

  • sudden death
  • lameness
  • seizure
  • arrhythmias
  • cold extremities

-Signs of Sepsis:

  • Pyrexia
  • Neck Pain
  • Joint Pain
  • Muscle Pain
  • Anorexia
  • Lethargy

-Signs of Cardiac Involvement:

  • Syncope
  • Weakness
  • Exercise Intolerance
  • Heart Failure
  • Pulmonary edema
  • Pulse deficits


Physical Exam

-Systolic Murmur (Mitral Valve Affected)

-Diastolic Murmur (Aortic Valve Affected)

-Pulmonary crackles (If edema is present)


Laboratory Findings

-Urine analysis

  • If UTI is present, could be (+/-) for the same bacteria that caused endocarditis
  • Proteinuria
  • Casts
  • Pyuria
  • Hematuria


-Blood Culture

  • collect blood from the jugular vein
  • 3-4 sterile samples taken 1 hour apart over 24 hours and grown in enhancement media
  • Positive culture (Rare)
  • Negative culture is not diagnostic


-Blood Profiles:

  • Hematology=leukocytosis, neutrophilia, monocytosis, nonregenerative anemia, thrombocytopenia (See with development of: disseminated intravascular coagulation); clotting times may be prolonged
  • Biochemistry=hypoalbumenemia, hypoglycemia (if septic), signs of complications from emboli


Radiography

-Usually normal unless severe damage is present

-Left atrial and ventricular enlargement (Mitral Valve Incompetence)

-Right atrial and ventricular enlargement (Aortic Valve Incompetence)

-Signs of congestive heart failure with chronic/severe valve damage


Electrocardiography (ECG)

-Usually normal

-Arrhythmias (especially ventricular premature complexes; AV node damage causes 3rd degree AV block)


Echocardiography

-Vegetative lesions on valves and/ mural surfaces


Treatment

-Antibiotic given I/V for at least five days and then given orally for at least six weeks (Broad Spectrum or Culture/Sensitivity)

-Manage secondary problems:

(e.g. septic shock, congestive heart failure, embolization, D.I.C.)


Prognosis

-Guarded

(Possibility of recurrent infections, embolic complications, congestive heart failure)